Control of cytokine-driven eosinophil migratory behavior by TGF-beta-induced protein (TGFBI) and periostin
Periostin, which is induced by interleukin (IL)-13, is an extracellular matrix (ECM) protein that supports αMβ2 integrin-mediated adhesion and migration of IL-5-stimulated eosinophils. Transforming growth factor (TGF)-β-induced protein (TGFBI) is a widely expressed periostin paralog known to support...
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| creator | Barretto, Karina T Swanson, Calvin M Nguyen, Christopher L Annis, Douglas S Esnault, Stephane J Mosher, Deane F Johansson, Mats W |
| description | Periostin, which is induced by interleukin (IL)-13, is an extracellular matrix (ECM) protein that supports αMβ2 integrin-mediated adhesion and migration of IL-5-stimulated eosinophils. Transforming growth factor (TGF)-β-induced protein (TGFBI) is a widely expressed periostin paralog known to support monocyte adhesion. Our objective was to compare eosinophil adhesion and migration on TGFBI and periostin in the presence of IL-5-family cytokines. Eosinophil adhesion after 1 h and random motility over 20 h in the presence of various concentrations of IL-5, IL-3, or granulocyte macrophage-colony stimulating factor (GM-CSF) were quantified in wells coated with various concentrations of TGFBI or periostin. Results were compared to video microscopy of eosinophils. Cytokine-stimulated eosinophils adhered equivalently well to TGFBI or periostin in a coating concentration-dependent manner. Adhesion was blocked by anti-αMβ2 and stimulated at the lowest concentration by GM-CSF. In the motility assay, periostin was more potent than TGFBI, the coating-concentration effect was bimodal, and IL-3 was the most potent cytokine. Video microscopy revealed that under the optimal coating condition of 5 μg/ml periostin, most eosinophils migrated persistently and were polarized and acorn-shaped with a ruffling forward edge and granules gathered together, in front of the nucleus. On 10 μg/ml periostin or TGFBI, more eosinophils adopted a flattened pancake morphology with dispersed granules and nuclear lobes, and slower migration. Conversion between acorn and pancake morphologies were observed. We conclude that TGFBI or periostin supports two modes of migration by IL-5 family cytokine-activated eosinophils. The rapid mode is favored by intermediate protein coatings and the slower by higher coating concentrations. We speculate that eosinophils move by haptotaxis up a gradient of adhesive ECM protein and then slow down to surveil the tissue. |
| doi_str_mv | 10.1371/journal.pone.0201320 |
| format | Article |
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N.</contributor><creatorcontrib>Barretto, Karina T ; Swanson, Calvin M ; Nguyen, Christopher L ; Annis, Douglas S ; Esnault, Stephane J ; Mosher, Deane F ; Johansson, Mats W ; Melo, Rossana C. N.</creatorcontrib><description>Periostin, which is induced by interleukin (IL)-13, is an extracellular matrix (ECM) protein that supports αMβ2 integrin-mediated adhesion and migration of IL-5-stimulated eosinophils. Transforming growth factor (TGF)-β-induced protein (TGFBI) is a widely expressed periostin paralog known to support monocyte adhesion. Our objective was to compare eosinophil adhesion and migration on TGFBI and periostin in the presence of IL-5-family cytokines. Eosinophil adhesion after 1 h and random motility over 20 h in the presence of various concentrations of IL-5, IL-3, or granulocyte macrophage-colony stimulating factor (GM-CSF) were quantified in wells coated with various concentrations of TGFBI or periostin. Results were compared to video microscopy of eosinophils. Cytokine-stimulated eosinophils adhered equivalently well to TGFBI or periostin in a coating concentration-dependent manner. Adhesion was blocked by anti-αMβ2 and stimulated at the lowest concentration by GM-CSF. In the motility assay, periostin was more potent than TGFBI, the coating-concentration effect was bimodal, and IL-3 was the most potent cytokine. Video microscopy revealed that under the optimal coating condition of 5 μg/ml periostin, most eosinophils migrated persistently and were polarized and acorn-shaped with a ruffling forward edge and granules gathered together, in front of the nucleus. On 10 μg/ml periostin or TGFBI, more eosinophils adopted a flattened pancake morphology with dispersed granules and nuclear lobes, and slower migration. Conversion between acorn and pancake morphologies were observed. We conclude that TGFBI or periostin supports two modes of migration by IL-5 family cytokine-activated eosinophils. The rapid mode is favored by intermediate protein coatings and the slower by higher coating concentrations. We speculate that eosinophils move by haptotaxis up a gradient of adhesive ECM protein and then slow down to surveil the tissue.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0201320</identifier><identifier>PMID: 30048528</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Adhesion ; Asthma ; Biology and Life Sciences ; Care and treatment ; Cell Adhesion ; Cell Adhesion Molecules - immunology ; Cell Migration Assays, Leukocyte ; Cell Movement ; Cloning ; Coating effects ; Coatings ; Colony-stimulating factor ; Cytokines ; Engineering and Technology ; Eosinophils ; Eosinophils - cytology ; Eosinophils - immunology ; Extracellular matrix ; Extracellular Matrix Proteins - immunology ; Granular materials ; Granulocyte-macrophage colony-stimulating factor ; Granulocyte-Macrophage Colony-Stimulating Factor - immunology ; Growth factors ; Humans ; Integrins ; Interleukin 3 ; Interleukin 5 ; Interleukin-3 - immunology ; Interleukin-5 - immunology ; Interleukins ; Kinases ; Leukocyte migration ; Leukocytes (eosinophilic) ; Leukocytes (granulocytic) ; Life Sciences ; Lung cancer ; Macrophages ; Medicine and Health Sciences ; Microscopy ; Monocytes ; Morphology ; Physical Sciences ; Physiological aspects ; Proteins ; Research and Analysis Methods ; Transforming Growth Factor beta - immunology ; Transforming growth factor-b ; Transforming growth factors</subject><ispartof>PloS one, 2018-07, Vol.13 (7), p.e0201320-e0201320</ispartof><rights>COPYRIGHT 2018 Public Library of Science</rights><rights>2018 Barretto et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>Attribution</rights><rights>2018 Barretto et al 2018 Barretto et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c627t-e575151ceb35275b4dfb5079ab65801c0a396e5295874e161f37023334d14f9c3</citedby><cites>FETCH-LOGICAL-c627t-e575151ceb35275b4dfb5079ab65801c0a396e5295874e161f37023334d14f9c3</cites><orcidid>0000-0001-5699-978X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6062114/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6062114/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,2102,2928,23866,27924,27925,53791,53793,79600,79601</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30048528$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://hal.univ-lille.fr/hal-04614218$$DView record in HAL$$Hfree_for_read</backlink></links><search><contributor>Melo, Rossana C. N.</contributor><creatorcontrib>Barretto, Karina T</creatorcontrib><creatorcontrib>Swanson, Calvin M</creatorcontrib><creatorcontrib>Nguyen, Christopher L</creatorcontrib><creatorcontrib>Annis, Douglas S</creatorcontrib><creatorcontrib>Esnault, Stephane J</creatorcontrib><creatorcontrib>Mosher, Deane F</creatorcontrib><creatorcontrib>Johansson, Mats W</creatorcontrib><title>Control of cytokine-driven eosinophil migratory behavior by TGF-beta-induced protein (TGFBI) and periostin</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Periostin, which is induced by interleukin (IL)-13, is an extracellular matrix (ECM) protein that supports αMβ2 integrin-mediated adhesion and migration of IL-5-stimulated eosinophils. Transforming growth factor (TGF)-β-induced protein (TGFBI) is a widely expressed periostin paralog known to support monocyte adhesion. Our objective was to compare eosinophil adhesion and migration on TGFBI and periostin in the presence of IL-5-family cytokines. Eosinophil adhesion after 1 h and random motility over 20 h in the presence of various concentrations of IL-5, IL-3, or granulocyte macrophage-colony stimulating factor (GM-CSF) were quantified in wells coated with various concentrations of TGFBI or periostin. Results were compared to video microscopy of eosinophils. Cytokine-stimulated eosinophils adhered equivalently well to TGFBI or periostin in a coating concentration-dependent manner. Adhesion was blocked by anti-αMβ2 and stimulated at the lowest concentration by GM-CSF. In the motility assay, periostin was more potent than TGFBI, the coating-concentration effect was bimodal, and IL-3 was the most potent cytokine. Video microscopy revealed that under the optimal coating condition of 5 μg/ml periostin, most eosinophils migrated persistently and were polarized and acorn-shaped with a ruffling forward edge and granules gathered together, in front of the nucleus. On 10 μg/ml periostin or TGFBI, more eosinophils adopted a flattened pancake morphology with dispersed granules and nuclear lobes, and slower migration. Conversion between acorn and pancake morphologies were observed. We conclude that TGFBI or periostin supports two modes of migration by IL-5 family cytokine-activated eosinophils. The rapid mode is favored by intermediate protein coatings and the slower by higher coating concentrations. We speculate that eosinophils move by haptotaxis up a gradient of adhesive ECM protein and then slow down to surveil the tissue.</description><subject>Adhesion</subject><subject>Asthma</subject><subject>Biology and Life Sciences</subject><subject>Care and treatment</subject><subject>Cell Adhesion</subject><subject>Cell Adhesion Molecules - immunology</subject><subject>Cell Migration Assays, Leukocyte</subject><subject>Cell Movement</subject><subject>Cloning</subject><subject>Coating effects</subject><subject>Coatings</subject><subject>Colony-stimulating factor</subject><subject>Cytokines</subject><subject>Engineering and Technology</subject><subject>Eosinophils</subject><subject>Eosinophils - cytology</subject><subject>Eosinophils - immunology</subject><subject>Extracellular matrix</subject><subject>Extracellular Matrix Proteins - immunology</subject><subject>Granular materials</subject><subject>Granulocyte-macrophage colony-stimulating factor</subject><subject>Granulocyte-Macrophage Colony-Stimulating Factor - immunology</subject><subject>Growth factors</subject><subject>Humans</subject><subject>Integrins</subject><subject>Interleukin 3</subject><subject>Interleukin 5</subject><subject>Interleukin-3 - immunology</subject><subject>Interleukin-5 - immunology</subject><subject>Interleukins</subject><subject>Kinases</subject><subject>Leukocyte migration</subject><subject>Leukocytes (eosinophilic)</subject><subject>Leukocytes (granulocytic)</subject><subject>Life Sciences</subject><subject>Lung cancer</subject><subject>Macrophages</subject><subject>Medicine and Health Sciences</subject><subject>Microscopy</subject><subject>Monocytes</subject><subject>Morphology</subject><subject>Physical Sciences</subject><subject>Physiological aspects</subject><subject>Proteins</subject><subject>Research and Analysis Methods</subject><subject>Transforming Growth Factor beta - immunology</subject><subject>Transforming growth factor-b</subject><subject>Transforming growth factors</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNptkl9r2zAUxc3YWLtu32Bshr20D870X_bLIAtrGwjspXsWknydKHOkTHIC-fZTGre0pfhB5up3ztW9nKL4jNEEU4m_r8Muet1PtsHDBBGEKUFvinPcUFIJgujbJ_9nxYeU1ghxWgvxvjijCLGak_q8WM-CH2Loy9CV9jCEv85D1Ua3B19CSM6H7cr15cYtox5CPJQGVnrvQizNoby7ua4MDLpyvt1ZaMttDAM4X17mm5_zq1L7XIPoQhqc_1i863Sf4NN4XhR_rn_dzW6rxe-b-Wy6qKwgcqiAS445tmAoJ5Ib1naGI9loI3iNsEWaNgI4aXgtGWCBOyoRoZSyFrOusfSi-Hry3fYhqXFNSREkJWUZFJmYn4g26LXaRrfR8aCCduq-EOJS6Tg424PC2DQarGiajjCDuJYG5-6saxshAWT2-jF225kNtBbyOnX_zPT5jXcrtQx7JZAgGLNscHUyWL2Q3U4X6lhDTGBGcL3Hmb0cm8XwbwdpUBuXLPS99hB29zPWvKaS1Bn99gJ9fRMjtdR5WOe7kN9oj6ZqypmsCRIYZWryCpW_FjbO5vx1LtefCdhJYGNIKUL3OBhG6pjeh8eoY3rVmN4s-_J0l4-ih7jS_0QL6i4</recordid><startdate>20180726</startdate><enddate>20180726</enddate><creator>Barretto, Karina T</creator><creator>Swanson, Calvin M</creator><creator>Nguyen, Christopher L</creator><creator>Annis, Douglas S</creator><creator>Esnault, Stephane J</creator><creator>Mosher, Deane F</creator><creator>Johansson, Mats W</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>1XC</scope><scope>VOOES</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0001-5699-978X</orcidid></search><sort><creationdate>20180726</creationdate><title>Control of cytokine-driven eosinophil migratory behavior by TGF-beta-induced protein (TGFBI) and periostin</title><author>Barretto, Karina T ; Swanson, Calvin M ; Nguyen, Christopher L ; Annis, Douglas S ; Esnault, Stephane J ; Mosher, Deane F ; Johansson, Mats W</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c627t-e575151ceb35275b4dfb5079ab65801c0a396e5295874e161f37023334d14f9c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Adhesion</topic><topic>Asthma</topic><topic>Biology and Life Sciences</topic><topic>Care and treatment</topic><topic>Cell Adhesion</topic><topic>Cell Adhesion Molecules - immunology</topic><topic>Cell Migration Assays, Leukocyte</topic><topic>Cell Movement</topic><topic>Cloning</topic><topic>Coating effects</topic><topic>Coatings</topic><topic>Colony-stimulating factor</topic><topic>Cytokines</topic><topic>Engineering and Technology</topic><topic>Eosinophils</topic><topic>Eosinophils - cytology</topic><topic>Eosinophils - immunology</topic><topic>Extracellular matrix</topic><topic>Extracellular Matrix Proteins - immunology</topic><topic>Granular materials</topic><topic>Granulocyte-macrophage colony-stimulating factor</topic><topic>Granulocyte-Macrophage Colony-Stimulating Factor - immunology</topic><topic>Growth factors</topic><topic>Humans</topic><topic>Integrins</topic><topic>Interleukin 3</topic><topic>Interleukin 5</topic><topic>Interleukin-3 - immunology</topic><topic>Interleukin-5 - immunology</topic><topic>Interleukins</topic><topic>Kinases</topic><topic>Leukocyte migration</topic><topic>Leukocytes (eosinophilic)</topic><topic>Leukocytes (granulocytic)</topic><topic>Life Sciences</topic><topic>Lung cancer</topic><topic>Macrophages</topic><topic>Medicine and Health Sciences</topic><topic>Microscopy</topic><topic>Monocytes</topic><topic>Morphology</topic><topic>Physical Sciences</topic><topic>Physiological aspects</topic><topic>Proteins</topic><topic>Research and Analysis Methods</topic><topic>Transforming Growth Factor beta - 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Academic</collection><collection>Hyper Article en Ligne (HAL)</collection><collection>Hyper Article en Ligne (HAL) (Open Access)</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>PloS one</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Barretto, Karina T</au><au>Swanson, Calvin M</au><au>Nguyen, Christopher L</au><au>Annis, Douglas S</au><au>Esnault, Stephane J</au><au>Mosher, Deane F</au><au>Johansson, Mats W</au><au>Melo, Rossana C. N.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Control of cytokine-driven eosinophil migratory behavior by TGF-beta-induced protein (TGFBI) and periostin</atitle><jtitle>PloS one</jtitle><addtitle>PLoS One</addtitle><date>2018-07-26</date><risdate>2018</risdate><volume>13</volume><issue>7</issue><spage>e0201320</spage><epage>e0201320</epage><pages>e0201320-e0201320</pages><issn>1932-6203</issn><eissn>1932-6203</eissn><abstract>Periostin, which is induced by interleukin (IL)-13, is an extracellular matrix (ECM) protein that supports αMβ2 integrin-mediated adhesion and migration of IL-5-stimulated eosinophils. Transforming growth factor (TGF)-β-induced protein (TGFBI) is a widely expressed periostin paralog known to support monocyte adhesion. Our objective was to compare eosinophil adhesion and migration on TGFBI and periostin in the presence of IL-5-family cytokines. Eosinophil adhesion after 1 h and random motility over 20 h in the presence of various concentrations of IL-5, IL-3, or granulocyte macrophage-colony stimulating factor (GM-CSF) were quantified in wells coated with various concentrations of TGFBI or periostin. Results were compared to video microscopy of eosinophils. Cytokine-stimulated eosinophils adhered equivalently well to TGFBI or periostin in a coating concentration-dependent manner. Adhesion was blocked by anti-αMβ2 and stimulated at the lowest concentration by GM-CSF. In the motility assay, periostin was more potent than TGFBI, the coating-concentration effect was bimodal, and IL-3 was the most potent cytokine. Video microscopy revealed that under the optimal coating condition of 5 μg/ml periostin, most eosinophils migrated persistently and were polarized and acorn-shaped with a ruffling forward edge and granules gathered together, in front of the nucleus. On 10 μg/ml periostin or TGFBI, more eosinophils adopted a flattened pancake morphology with dispersed granules and nuclear lobes, and slower migration. Conversion between acorn and pancake morphologies were observed. We conclude that TGFBI or periostin supports two modes of migration by IL-5 family cytokine-activated eosinophils. The rapid mode is favored by intermediate protein coatings and the slower by higher coating concentrations. We speculate that eosinophils move by haptotaxis up a gradient of adhesive ECM protein and then slow down to surveil the tissue.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>30048528</pmid><doi>10.1371/journal.pone.0201320</doi><orcidid>https://orcid.org/0000-0001-5699-978X</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2018-07, Vol.13 (7), p.e0201320-e0201320 |
| issn | 1932-6203 1932-6203 |
| language | eng |
| recordid | cdi_plos_journals_2077342336 |
| source | MEDLINE; DOAJ Directory of Open Access Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Public Library of Science (PLoS) Journals Open Access; PubMed Central; Free Full-Text Journals in Chemistry |
| subjects | Adhesion Asthma Biology and Life Sciences Care and treatment Cell Adhesion Cell Adhesion Molecules - immunology Cell Migration Assays, Leukocyte Cell Movement Cloning Coating effects Coatings Colony-stimulating factor Cytokines Engineering and Technology Eosinophils Eosinophils - cytology Eosinophils - immunology Extracellular matrix Extracellular Matrix Proteins - immunology Granular materials Granulocyte-macrophage colony-stimulating factor Granulocyte-Macrophage Colony-Stimulating Factor - immunology Growth factors Humans Integrins Interleukin 3 Interleukin 5 Interleukin-3 - immunology Interleukin-5 - immunology Interleukins Kinases Leukocyte migration Leukocytes (eosinophilic) Leukocytes (granulocytic) Life Sciences Lung cancer Macrophages Medicine and Health Sciences Microscopy Monocytes Morphology Physical Sciences Physiological aspects Proteins Research and Analysis Methods Transforming Growth Factor beta - immunology Transforming growth factor-b Transforming growth factors |
| title | Control of cytokine-driven eosinophil migratory behavior by TGF-beta-induced protein (TGFBI) and periostin |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-28T19%3A02%3A06IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Control%20of%20cytokine-driven%20eosinophil%20migratory%20behavior%20by%20TGF-beta-induced%20protein%20(TGFBI)%20and%20periostin&rft.jtitle=PloS%20one&rft.au=Barretto,%20Karina%20T&rft.date=2018-07-26&rft.volume=13&rft.issue=7&rft.spage=e0201320&rft.epage=e0201320&rft.pages=e0201320-e0201320&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0201320&rft_dat=%3Cgale_plos_%3EA547820610%3C/gale_plos_%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2077342336&rft_id=info:pmid/30048528&rft_galeid=A547820610&rft_doaj_id=oai_doaj_org_article_11b9aec699f24b05a7b16e54fd967ee7&rfr_iscdi=true |